Effect of secretin on electrical activity of small intestine

1975 ◽  
Vol 229 (2) ◽  
pp. 484-488 ◽  
Author(s):  
AK Mukhopadhyay ◽  
LR Johnson ◽  
EM Copeland ◽  
NW Weisbrodt

The effect of intravenously administered secretin (0.5, 2.0, 6.0 U/kg-h) and intraduodenal acidification (13.2 meq/h HCl) on the electrical activity of the small bowel of three conscious dogs with gastric and duodenal cannulas was observed. Electrical activity was recorded in fasted as well as fed conditions through silver wire electrodes implanted along the entire length of the small bowel. Intravenous infusion of secretin in all dosages and in all dogs delayed the onset of the interdigestive myoelectric complex and reduced the total percentage of slow waves with superimposed spike potentials. Intraduodenal acidification also inhibited the interdigestive myoelectric complex, which developed incompletely with fewer action potentials on slow waves. Secretin did not produce any alteration in the fed pattern of activity, slow-wave frequency, or the caudal migration of the interdigestive myoelectric complex. The present study indicates that the nuerohumoral mechanisms responsible for initiation of the interdigestive myoelectric complex may be different from those responsible for its caudal migration.

1993 ◽  
Vol 265 (4) ◽  
pp. G619-G627
Author(s):  
W. C. De Vos

This study characterizes the migrating spike complex (MSC) in the small intestine of the awake fasting cat and compares the MSC with interdigestive activity in the small intestine of other species. Electrical activity in each of 12 cats with implanted electrodes showed MSCs, bands of spike potentials which attenuated slow-wave frequency and amplitude as the MSCs progressed distally. MSCs occurred at variable frequency with intervals ranging from < 1 min to > 5 h and averaged 51.2 +/- 2.8 (SE) min. MSCs migrated at 1-8 mm/s, accelerating distally; the duration decreased distally such that the length of the bowel in a burst (2-3 cm proximally) was conserved. The MSC was associated with an intense prolonged contraction of duration similar to that of the MSC. Sometimes the MSCs occurred in close association, and when an MSC period was < 5.7 min, the second MSC propagated at a slower rate than the first. Frequently, a brief series of slow wave-associated spikes preceded an MSC. MSCs were not associated with slow waves. The MSC differs in several respects from the migrating myoelectric complex of other laboratory animals and is more appropriately classified in a category that includes giant migrating spikes, prolonged propagated contractions, power contractions, and migrating action potential complexes.


1960 ◽  
Vol 38 (7) ◽  
pp. 777-801 ◽  
Author(s):  
E. E. Daniel ◽  
B. T. Wachter ◽  
A. J. Honour ◽  
A. Bogoch

Electrical activity of the small intestine of man and of dogs has been studied using monopolar recording techniques and spread of electrical activity in the small intestine of the dog using a bipolar recording technique. Motility was studied simultaneously. Electrical activity consisted of slow waves and action potentials which occurred when contractions were present. Action potentials were not conducted but slow waves sometimes spread aborally for short distances. Particular attention was paid to the relation of slow waves to action potentials and to motility. No consistent alteration in the frequency or configuration of slow waves was found associated with the occurrence of action potentials and motility, although serotonin or epinephrine altered slow wave frequency slightly. Slow waves usually were increased in amplitude during periods when motility and action potentials were occurring (during eating or balloon propulsion; after the administration of serotonin, neostigmine, physostigmine, or morphine). Slow wave amplitudes usually were diminished when motility was inhibited (by balloon distention; after administration of epinephrine, etc.). Action potentials tended to occur in phase with the slow waves, when the muscle electrode was positive relative to the indifferent electrode, but this was not always so during nonpropulsive contractions. There was also a correlation between the occurrence of distal spread of slow waves over the duodenum and upper jejunum and the ability of the intestine in this region to respond to balloon distention by propulsion.In the dog, body temperature consistently affected slow waves. A decrease of 10 °C diminished their frequencies to less than one-half and diminished their amplitude. Slow waves occurred at similar frequencies and with regular conduction after large doses of nicotine or atropine. Dibenzyline, dichloroisopropyl-norepinephrine, and vagotomy did not markedly alter slow wave frequencies. These findings and those in our studies with microelectrodes indicate that the slow waves are myogenic in origin, and represent electrical currents in the extracellular fluid initiated by periodic depolarizations of muscle cells of the small intestine.


1960 ◽  
Vol 38 (1) ◽  
pp. 777-801 ◽  
Author(s):  
E. E. Daniel ◽  
B. T. Wachter ◽  
A. J. Honour ◽  
A. Bogoch

Electrical activity of the small intestine of man and of dogs has been studied using monopolar recording techniques and spread of electrical activity in the small intestine of the dog using a bipolar recording technique. Motility was studied simultaneously. Electrical activity consisted of slow waves and action potentials which occurred when contractions were present. Action potentials were not conducted but slow waves sometimes spread aborally for short distances. Particular attention was paid to the relation of slow waves to action potentials and to motility. No consistent alteration in the frequency or configuration of slow waves was found associated with the occurrence of action potentials and motility, although serotonin or epinephrine altered slow wave frequency slightly. Slow waves usually were increased in amplitude during periods when motility and action potentials were occurring (during eating or balloon propulsion; after the administration of serotonin, neostigmine, physostigmine, or morphine). Slow wave amplitudes usually were diminished when motility was inhibited (by balloon distention; after administration of epinephrine, etc.). Action potentials tended to occur in phase with the slow waves, when the muscle electrode was positive relative to the indifferent electrode, but this was not always so during nonpropulsive contractions. There was also a correlation between the occurrence of distal spread of slow waves over the duodenum and upper jejunum and the ability of the intestine in this region to respond to balloon distention by propulsion.In the dog, body temperature consistently affected slow waves. A decrease of 10 °C diminished their frequencies to less than one-half and diminished their amplitude. Slow waves occurred at similar frequencies and with regular conduction after large doses of nicotine or atropine. Dibenzyline, dichloroisopropyl-norepinephrine, and vagotomy did not markedly alter slow wave frequencies. These findings and those in our studies with microelectrodes indicate that the slow waves are myogenic in origin, and represent electrical currents in the extracellular fluid initiated by periodic depolarizations of muscle cells of the small intestine.


2001 ◽  
Vol 280 (3) ◽  
pp. G491-G500 ◽  
Author(s):  
Graeme Donnelly ◽  
Timothy D. Jackson ◽  
Krista Ambrous ◽  
Jing Ye ◽  
Adeel Safdar ◽  
...  

In an in vitro model for distention-induced peristalsis in the guinea pig small intestine, the electrical activity, intraluminal pressure, and outflow of contents were studied simultaneously to search for evidence of myogenic control activity. Intraluminal distention induced periods of nifedipine-sensitive slow wave activity with superimposed action potentials, alternating with periods of quiescence. Slow waves and associated high intraluminal pressure transients propagated aborally, causing outflow of content. In the proximal small intestine, a frequency gradient of distention-induced slow waves was observed, with a frequency of 19 cycles/min in the first 1 cm and 11 cycles/min 10 cm distally. Intracellular recording revealed that the guinea pig small intestinal musculature, in response to carbachol, generated slow waves with superimposed action potentials, both sensitive to nifedipine. These slow waves also exhibited a frequency gradient. In addition, distention and cholinergic stimulation induced high-frequency membrane potential oscillations (∼55 cycles/min) that were not associated with distention-induced peristalsis. Continuous distention produced excitation of the musculature, in part neurally mediated, that resulted in periodic occurrence of bursts of distally propagating nifedipine-sensitive slow waves with superimposed action potentials associated with propagating intraluminal pressure waves that caused pulsatile outflow of content at the slow wave frequency.


1999 ◽  
Vol 77 (8) ◽  
pp. 598-605 ◽  
Author(s):  
Rosa Espinosa-Luna ◽  
Stephen M Collins ◽  
Luis M Montaño ◽  
Carlos Barajas-López

Intracellular recordings were obtained to investigate whether slow wave and spike type action potentials are present in cell cultures of the muscularis externa from the guinea pig small intestine. The muscularis externa of the small intestine was dissociated by using specific purified enzymes and gentle mechanical dissociation. Cells were plated on cover slips and maintained in culture for up to 4 weeks. Dissociated cells obtained in this way reorganized themselves in a few days to form small cell clumps showing spontaneous movements. Intracellular recordings of these clumps displayed both spike and slow wave type action potentials. Spikes were observed on top of some slow waves and were abolished by the addition of nifedipine or the removal of extracellular calcium. Slow waves, however, were nifedipine insensitive and temperature sensitive, and were abolished by octanol (a gap junction blocker) and forskolin (an adenyl cyclase activator). Slow waves were never observed in small clumps (<50 µm), suggesting that a critical mass of cells might be required for their generation. These observations demonstrated for the first time the presence of nifedipine-insensitive slow waves in cell cultures of the muscularis externa from the guinea pig small intestine. Cell cultures allow rigorous control of the immediate environment for the cells and this should facilitate future studies on the molecular and cellular mechanisms responsible for the slow waves in the gastrointestinal tract.Key words: smooth muscle, slow waves, spiking activity, gastrointestinal tract, gut, small intestine, electrophysiology, pacemaker activity, guinea pig.


1995 ◽  
Vol 73 (10) ◽  
pp. 1502-1511 ◽  
Author(s):  
John Malysz ◽  
David Richardsons ◽  
Laura Farraway ◽  
Jan D. Huizinga ◽  
Marie-Odile Christen

Intrinsic electrical activities in various isolated segments of the mouse small intestine were recorded (i) to characterize action potential generation and (ii) to obtain a profile on the ion channels involved in initiating the slow wave type action potentials (slow waves). Gradients in slow wave frequency, resting membrane potential, and occurrence of spiking activity were found, with the proximal intestine exhibiting the highest frequency, the most hyperpolarized cell membrane, and the greatest occurrence of spikes. The slow waves were only partially sensitive to L-type calcium channel blockers. Nifedipine, verapamil, and pinaverium bromide abolished spikes that occurred on the plateau phase of the slow waves in all tissues. The activity that remained in the presence of L-type calcium channel blockers, the upstroke potential, retained a similar amplitude to the original slow wave and was of identical frequency. The upstroke potential was not sensitive to a reduction in extracellular chloride or to the sodium channel blockers tetrodotoxin and mexiletine. Abolishment of the Na+ gradient by removal of 120 mM extracellular Na+ reduced the upstroke potential frequency by 13–18% and its amplitude by 50–70% in the ileum. The amplitude was similarly reduced by Ni2+ (up to 5 mM), and by flufenamic acid (100 μM), a nonspecific cation and chloride channel blocker. Gadolinium, a nonspecific blocker of cation and stretch-activated channels, had no effect. Throughout these pharmacological manipulations, a robust oscillation remained at 5–10 mV. This oscillation likely reflects pacemaker activity. It was rapidly abolished by removal of extracellular calcium but not affected by L-type calcium channel blockers. In summary, the mouse small intestine has been established as a model for research into slow wave generation and electrical pacemaker activity. The upstroke part of the slow wave has two components, the pacemaker component involves a non-L-type calcium channel.Key words: slow wave, pacemaker, calcium channel, pinaverium, smooth muscle.


1961 ◽  
Vol 201 (1) ◽  
pp. 209-212 ◽  
Author(s):  
Alex Bortoff

The effects of certain autonomic and metabolic drugs on the electrical activity of the small intestine have been investigated, using the pressure electrode. Epinephrine inhibits spike activity and increases the membrane potential, without apparently altering the size of the slow waves. Acetylcholine has the reverse effect. The hyperpolarization produced by epinephrine is followed by a gradual depolarization which exceeds that of the membrane prior to its addition; this is not accompanied by the reappearance of spike activity. Large concentrations of epinephrine produce a waxing and waning of the amplitude of the slow waves. During inhibition by dinitrophenol, both acetylcholine and epinephrine can initiate slow wave activity. An explanation of naturally occurring waxing and waning is suggested, together with a mechanism relating the activity of the two muscle layers during normal intestinal motility.


1980 ◽  
Vol 239 (5) ◽  
pp. G406-G410 ◽  
Author(s):  
J. S. Gidda ◽  
R. K. Goyal

Experiments were performed in anesthetized opossums to study the nature of vagal control on the small bowel. Electrical activity was recorded in the duodenum, jejunum, and ileum with silver chloride electrodes. Slow waves and spike potentials were observed at all three sites. There was a decreasing frequency gradient of slow waves and the incidence of slow waves with spikes in the aboral direction. Vagotomy had no effect on the electrical activity. Vagal stimulation at threshold stimuli inhibited spike potentials in all three segments of small intestine, but slow waves were not affected. Vagal stimulation after sectioning of the gut proximal to the electrodes converted the response from inhibition to excitation. These studies suggest that a) vagus carries both excitatory and inhibitory influences to the small bowel; b) inhibitory influences are dominant in the intact opossum small intestine; and c) the nature of the response obtained with vagal stimulation may be explained on the basis of the paths taken by inhibitory and excitatory fibers.


1982 ◽  
Vol 48 (1) ◽  
pp. 129-135 ◽  
Author(s):  
Maurice Roche ◽  
Lionel Bueno ◽  
Monique Vagne ◽  
Christian Blourde

1. Bipolar electrodes were permanently implanted on the gastric antrum, and on the different portions of the small intestine of each of eleven healthy adult cats receiving one meal daily. All parts of the feline gut exhibited, as in several other species, regular slow waves and alternate periods of quiescence and electrical spiking activity during the recording sessions lasting from 10 to 30 d.2. Patterns of electrical activity characteristic of this species were identified. Both the amplitude and frequency of the antral slow-wave were related to the presence cf superimposed spike bursts during fasting decrease in the antral slow-wave frequency and increase in the length of the duodenal plateau of slow waves after the daily meal were related to its nature.3. In fasted state, the electrical spiking activity of the small intestine occurred as fused spike bursts of large amplitude potentials migrating slowly over short distances only 24 h after feeding. They are interspersed with short periods of irregular spiking activity.4. These findings suggested that, except the distal part of the small intestine which showed an activity which resembled partially the migrating myoelectric complex observed in other species during the fasting state, the motility patterns of the digestive tract in the cat were not comparable to those observed in the dog or sheep. In the cat, mixing of the contents seemed to result from more or less regular spiking activity allowing their propulsion distally. The propagation over distances varying from 200 to 1000 mm of nine to eighteen daily fused spike bursts in the fasting state remains unclear but they are related to the digestive function in accordance with the displacement aborally of their origin in a prolonged fasting condition.


2001 ◽  
Vol 280 (3) ◽  
pp. G439-G448 ◽  
Author(s):  
John Malysz ◽  
Graeme Donnelly ◽  
Jan D. Huizinga

Slow waves determine frequency and propagation characteristics of contractions in the small intestine, yet little is known about mechanisms of slow wave regulation. We propose a role for intracellular Ca2+, inositol 1,4,5,-trisphosphate (IP3)-sensitive Ca2+ release, and sarcoplasmic reticulum (SR) Ca2+ content in the regulation of slow wave frequency because 1) 1,2-bis(2-aminophenoxy)ethane- N,N,N′,N′-tetraacetic acid-AM, a cytosolic Ca2+ chelator, reduced the frequency or abolished the slow waves; 2) thapsigargin and cyclopiazonic acid (CPA), inhibitors of SR Ca2+-ATPase, decreased slow wave frequency; 3) xestospongin C, a reversible, membrane-permeable blocker of IP3-induced Ca2+release, abolished slow wave activity; 4) caffeine and phospholipase C inhibitors (U-73122, neomycin, and 2-nitro-4-carboxyphenyl- N, N-diphenylcarbamate) inhibited slow wave frequency; 5) in the presence of CPA or thapsigargin, stimulation of IP3 synthesis with carbachol, norepinephrine, or phenylephrine acting on α1-adrenoceptors initially increased slow wave frequency but thereafter increased the rate of frequency decline, 6) thimerosal, a sensitizing agent of IP3 receptors increased slow wave frequency, and 7) ryanodine, a selective modulator of Ca2+-induced Ca2+ release, had no effect on slow wave frequency. In summary, these data are consistent with a role of IP3-sensitive Ca2+ release and the rate of SR Ca2+ refilling in regulation of intestinal slow wave frequency.


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